NOVEL ANION DEPENDENCE OF INDUCED CATION-TRANSPORT IN MALARIA-INFECTED ERYTHROCYTES

Following invasion by the malaria parasite there appear in the parasit ized erythrocyte new (''induced''') permeation pathways that mediate t he transport of a wide variety of small solutes, Although anion-select ive, these pathways have a significant cation permeability and cause a substantial increase in the basal leak of cations into and out of the infected cell. In this study of human erythrocytes infected in vitro with Plasmodium falciparum it was shown that the transport of monovale nt cations (Rb+ and choline), but not that of a nonelectrolyte (sorbit ol) or a monovalent anion (lactate), via the malaria induced pathways is strongly dependent on the nature of the anion in the suspending med ium. Substitution of NO3- for Cl- resulted in a 4-6-fold increase in t he unidirectional influx and efflux of Rb+, and a 2-3-fold increase in the influx of choline via the induced pathways, By contrast, replacem ent of Cl- with NO3- caused a slight (although not significant) decrea se in the malaria-induced influx of sorbitol and lactate, Hemolysis ex periments with a range of K+ salts revealed that the net influx of Kinto infected cells showed the same novel anion dependence as seen for the unidirectional flux of Rb+ and choline, with hemolysis occurring much faster in iso-osmotic KNO3 and KSCN solutions than in KCl, KBr, o r KI solutions, Hemolysis in the corresponding Na+ salt solutions was very much slower, consistent with the induced pathways being selective for K+ over Na+, and raising the possibility that the efflux of cell K+ via these pathways may play a role in host cell volume regulation. A number of models that would account for the anion dependence of mala ria-induced cation transport are considered.